Failure of fixation suppression

Alpert, Jack N.

doi:10.1212/wnl.24.9.891

Cited by 66 publications

(26 citation statements)

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“…The percentage reduction calculated with slow-phase velocity best distinguished nor mal from abnormal visual fixation which is in agreement with previous reports [Alpert, 1974;, However, if a ±5% safety margin is taken into account around the line of 60% reduction in slow-phase ve locity, determined as the lower limit for the normals in a previous report , the number of false-negatives in creased in this area ( fig. 7).…”

Section: Discussionsupporting

confidence: 92%

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Visual Fixation of Caloric Nystagmus with Special Reference to a New Index

Kato¹,

Watanabe²,

Nakamura³

et al. 1984

ORL

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The effects of visual fixation upon caloric nystagmus were computed in each parameter as a measure. The percentage reduction established with slow-phase velocity best distinguished normal from abnormal visual fixation at the line of 60%. However, if a ± 5% safety margin is taken into account, 11 of 176 ears showed false-negatives. The number of nystagmus beats in normals decreased markedly during the period of fixation. In abnormals, the number of nystagmus beats increased definitely during the fixation period. Based on this fact, the product of slow-phase velocity multiplied by the number of nystagmus beats was assessed as the fixation-suppression index. As a result, 11 ears showing false-negative slow-phase velocity decreased to 2 ears. Thus, this modified fixation-suppression index seems to be an appropriate parameter to separate normal from abnormal fixation-suppression of caloric nystagmus.

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Section: Discussionsupporting

confidence: 92%

“…This phenome non was also reported in a previous paper [Alpert, 1974], Based on this fact, the product of the number of nystagmus beats multiplied by slow-phase velocity, i.e., the fixation-sup pression index, is a newly developed index to separate normal from abnormal fixation-sup pression of caloric nystagmus ( fig. 7-9).…”

Section: Discussionsupporting

confidence: 76%

Visual Fixation of Caloric Nystagmus with Special Reference to a New Index

Kato¹,

Watanabe²,

Nakamura³

et al. 1984

ORL

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“…Failure of fixation suppression of caloric nystagmus can be seen in central disorders such as cerebellar disease. In our study, all cases of fixation failure were associated with cerebellar infarction as in a previous study [20]. PAN is demonstrated by a periodic reversal of horizontal SN with a null period of several seconds.…”

Section: Discussionsupporting

confidence: 77%

Nystagmus-Based Approach to Vertebrobasilar Stroke Presenting as Vertigo without Initial Neurologic Signs

Kim

Boo²,

Ban³

2013

Eur Neurol

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Background: We aimed to investigate the clinical courses and common nystagmus of isolated vertigo patients with vertebrobasilar stroke. Methods: The patients who presented with isolated acute spontaneous vertigo with spontaneous nystagmus (acute vestibular syndrome) at the Emergency Department were retrospectively analyzed. They were referred to the Otolaryngology Department due to the absence of neurologic signs or even of imaging abnormalities after the initial examination at the Emergency Department. Various clinical features, including presenting symptoms, delayed neurologic signs, the site of infarction, and videonystagmographic (VNG) findings were analyzed. Results: Of the 468 cases of acute vestibular syndrome, 23 (4.9%) cases of radiologically proven vertebrobasilar stroke were identified. Of the 23 patients, 17 (74%) showed aggravation of vertigo or delayed neurologic signs during the admission. In the analysis of VNG, 11 (48%) cases of direction-changing gaze-evoked nystagmus, 7 (30%) cases of fixation failure in the caloric test, 6 (27%) cases of periodic alternating nystagmus, and 4 (17%) cases of atypical head-shaking nystagmus were presented. Stroke occurred in the cerebellum (n = 18, 78%), medulla (n = 4, 17%), and pons (n = 1, 4%). Conclusion: In the early stage of vertebrobasilar stroke, an accurate diagnosis was difficult in the Emergency Department even though a radiologic study was performed, but various VNG abnormalities and delayed neurologic signs could help to diagnose whether the origin is central or not.

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“…Results of certain clinical studies have suggested that inability to suppress visually an induced vestibular nystagmus (Ledoux and Demanez, 1970;Alpert, 1974;Takemori, 1977;Zee, 1977;Dichgans et al, 1978) or a spontaneous nystagmus (Hood, 1968) is a sign of central nervous disease. Others have maintained that similar significance can be attached to a derangement of the pursuit reflexes (Baloh et al, 1977).…”

mentioning

confidence: 99%